Chapter 10. Emergency Room Treatment

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DOI: 10.1176/appi.books.9781585622825.238759

Manual of Clinical Psychopharmacology >

Chapter 10. Emergency Room Treatment

INTRODUCTION

Psychiatrists see patients in crisis not only in emergency rooms (ERs) but also (occasionally) in

their offices, during home visits, or in medical or nursing home settings. In this chapter, we

address some of the more common emergencies facing the clinical psychiatrist.

In emergency situations, psychiatrists are often faced with the diagnosis and treatment of patients

presenting with psychiatric symptoms of sudden or presumed recent onset. Phenomenologically,

these symptoms can be crudely subdivided into the following types:

1. Agitation and violent behavior, with or without signs of alcohol or other intoxication
2. Depression with suicidal ideation, with or without a recent suicide attempt

Acute psychotic reactions, usually with overt thought disorder, paranoid ideation, and/or hallucinations

and marked fear or anger

3.  
4. Delirium presenting with disorientation and confusion, with or without psychotic symptoms
5. Severe anxiety without psychotic symptoms but often with physical symptoms
6. Psychogenic stupor/catatonia

In some of these situations a history can be obtained either from the patient or from friends or

relatives. Sometimes the patient may be carrying enough identification that friends or relatives can

be rapidly contacted. In the worst situation, the psychiatrist will have little to go on besides the

patient’s behavior and a brief physical examination. When the patient is severely disturbed,

obtunded, or confused, can give no history, and has no diagnostic stigmata (e.g., needle tracks,

obvious atropine-like toxic signs), hospitalization without specific drug treatment, or at least

medical evaluation with toxic screens, electrocardiogram, and so forth in a competent medical

emergency facility, is indicated.

We stress the importance of trying to ascertain which drugs the patient has been taking or may

have been taking before pharmacotherapy is begun. Deaths have occurred when a tricyclic

antidepressant (TCA) or meperidine was given to patients who were already taking monoamine

oxidase inhibitors (MAOIs). Adding sedative drugs in a patient already intoxicated on alcohol or

other sedative drugs is unwise. Adding a neuroleptic in a patient with possible neuroleptic

malignant syndrome (NMS) is obviously contraindicated. Similarly, drugs must be carefully chosen

if a TCA overdose may have affected cardiac function. In short, when the patient may have been

taking preexisting medication or may have overdosed on an unknown drug, it is better to avoid

medication until the situation can be clarified.

AGITATION AND VIOLENCE

Few ER encounters are more difficult than having to contend with an agitated, violent patient.

Individuals representing many diagnostic groups may present to the ER in an agitated, violent

state. In one survey, 80% of teaching hospital ERs reported patient assaults of staff members, and

at least 25% of these ERs had to restrain patients daily (Lavoie et al. 1988). Violence often

represents an attempt by the patient to assert control in the context of feeling frightened and

helpless.

In nonpsychotic patients presenting in ERs with angry tantrums, as well as in similar patients with

severe anxiety that seems to be based on family fights or other interpersonal crises, supportive

listening, reassurance, and the elixir of time often enable the patient to gradually become calm and

reasonable without specific medication. Sedative- or alcohol-related angry intoxication also often

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From the legal perspective, the use of external restraints is generally considered a less invasive

intervention than the involuntary administration of psychotropic medications. No intervention is

more effective for potentially violent patients than a sufficient show of force to restrain the patient,

if necessary, along with calm reassurance. Thus, this option should be employed if the patient

represents an imminent danger to himself or herself or others. However, some patients are quite

capable of exhausting or injuring themselves while in restraints. In these cases the addition of

medications is frequently required.

A number of open-label studies have investigated the use of various psychotropic agents in the

“rapid tranquilization” of agitated patients. Dr. William Dubin of Temple University has used that

term to describe the use of antipsychotics and benzodiazepines given every half hour or hour to

treat the target symptoms of agitation, motor excitement, tension, and hostility. Rapid

tranquilization is sometimes confused with rapid neuroleptization, which uses large loading doses

of antipsychotics, sometimes as much as 100 mg/day of haloperidol, in an attempt to accelerate

remission of psychotic symptoms. Unfortunately, studies have revealed that this strategy is not

successful, and side effects are burdensome. Rapid tranquilization strategies have been studied

with both psychotic and nonpsychotic patients.

The typical rapid tranquilization approach employs an intramuscular route of administration for

rapid absorption and increased bioavailability (Table 10–1). However, Dubin et al. (1985)

suggested that oral concentrate forms of antipsychotics also provide rapid response and may

decrease feelings of helplessness in an already vulnerable patient, relative to being approached

with a needle. In a study of 159 agitated psychiatric patients randomized to either intramuscular or

oral concentrate forms of thiothixene, haloperidol, or thioridazine, there was a minimal time

advantage to using the intramuscular route of administration, but fewer intramuscular doses were

required to achieve a satisfactory response (Dubin et al. 1985). In medical-surgical patients, the

intravenous route of administration is also a common option. Moller et al. (1982) found that

patients given intravenous haloperidol improved more rapidly than patients taking oral haloperidol

in the first 3 hours. However, after 3 hours there was no significant difference between the oral

and the intravenous haloperidol–treated groups. Several other open-label studies have confirmed

the utility of intravenous haloperidol and benzodiazepines (lorazepam) in the management of

agitated medical-surgical patients.

Table 10–1. Medication options for rapid tranquilization of agitated patients (administered every

30–60 minutes)

Medication

Dose

Average total dose for tranquilization

Intramuscular Oral

haloperidol 2.5–5 mg 5–10 mg 10–20 mg

thiothixene 10–20 mg 5–10 mg 15–30 mg

droperidol 2.5–5 mg Not available 5–20 mg

loxapine 10–15 mg 25 mg 30–60 mg

chlorpromazine 50 mg 100 mg 300–600 mg

lorazepam 0.5–1 mg 1–2 mg 4–8 mg

diazepam Not applicable 5–10 mg 20–60 mg

olanzapine 2.5–10 mg 2.5–5 mg 10–20 mg

ziprasidone 10–20 mg 40–160 mg 10–20 mg

aripiprazole 9.75 mg 10–30 mg 9.75–19.5 mg

Intramuscular atypicals such as intramuscular olanzapine, aripiprazole, and ziprasidone may well

replace intramuscular typicals such as haloperidol. However, if they do so, it will not likely be

because of superior efficacy. Rather the advantage of intramuscular atypicals may be in reducedPrint: Chapter 10. Emergency Room Treatment http://www.psychiatryonline.com/popup.aspx?aID=238762&print=yes…

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acute extrapyramidal symptoms (EPS). On the other hand, a significant disadvantage of the

atypical intramuscular formulations is that they are substantially more costly than generic agents

such as haloperidol. Intramuscular olanzapine has now been approved for use in treating agitation

associated with psychosis. It has been studied in the acute management of schizophrenia,

dementia, and bipolar disorder. In acutely agitated patients with dementia, olanzapine at 2.5 or 5

mg im was significantly more effective than placebo in reducing agitation 2 and 24 hours

postinjection (lorazepam at 1 mg was not) (Meehan et al. 2002). In patients with schizophrenia,

olanzapine at 5–10 mg im was significantly more effective than placebo at 2 and 24 hours

postinjection (Breier et al. 2001); similar data at 10–25 mg were observed in acutely manic

patients (Meehan et al. 2001). The primary advantages of intramuscular olanzapine over

intramuscular haloperidol are a faster onset of action and less EPS (Wright et al. 2003). The onset

of action of intramuscular olanzapine is within 30 minutes, and minimal EPS have been reported.

The most common side effects were somnolence and dizziness. Occasional mild hypotension and

bradycardia have been reported.

An injectable form of ziprasidone has been available since 2002. Ziprasidone has been evaluated in

several double-blind trials in the treatment of acute agitation. Both 10 mg and 20 mg im appear to

be effective, but 2 mg im was not effective. Like olanzapine, intramuscular ziprasidone has a low

incidence of EPS. In studies of acute agitation in psychotic patients, dosages of 10–20 mg/day

were as effective as haloperidol in treating agitation and more effective in treating psychosis. The

most common side effects with intramuscular ziprasidone were headache, nausea, and somnolence.

Aripiprazole became the latest atypical antipsychotic to be indicated in the treatment of acute

agitation associated with bipolar disorder, schizoaffective disorder, and schizophrenia. Several

studies of the acute effects of aripiprazole in the reduction of agitation have demonstrated the

superiority of this agent to placebo and its equivalence to intramuscular haloperidol (Andrezina et

1. 2006a, 2006b). Intramuscular aripiprazole appears to produce EPS much less commonly than

does intramuscular haloperidol, with about 2% of aripiprazole-treated patients experiencing

akathisia and 1% experiencing dystonic reactions. It is likely, but untested, that repeated doses

may increase the risk of EPS. Other side effects more commonly seen with intramuscular

aripiprazole than with placebo include headache, somnolence, nausea, and dizziness.

For severely agitated or imminently violent patients, rapid tranquilization strategies employ

antipsychotics every 30–60 minutes until the target symptoms of hostility, agitation, and

assaultiveness are reduced. Most studies suggest that the typical dose of antipsychotics required is

in the range of 300–600 mg of chlorpromazine, 10–20 mg of haloperidol, or 10–20 mg of

olanzapine over a 2- to 4-hour period (see Table 10–1). The high-potency typical antipsychotics

have the advantage of not producing significant adrenergic blockade in the acute setting. However,

akathisia and dystonic reactions may be problematic at higher doses, particularly in young males.

We have found that alternating the antipsychotic with a benzodiazepine is also a sound strategy. In

a common regimen, haloperidol 5 mg im is alternated with lorazepam 1–2 mg im every 30 minutes

until tranquilization is achieved. Droperidol was sometimes used for rapid tranquilization but has

now received a black box warning secondary to QTc prolongation. Droperidol is also associated with

hypotension and respiratory depression. Thus, its use in psychiatric settings is rarely warranted.

Lorazepam is the only benzodiazepine reliably absorbed from all routes of administration. However,

for oral dosing, diazepam may offer the most rapid onset of action. The combination of

benzodiazepines and antipsychotics offers several advantages. Frequently, lower doses of both

classes of medications are sufficient when they are combined. The lower doses decrease the risks

of side effects from either the benzodiazepines or the antipsychotics. Further, benzodiazepines may

counter some neuroleptic side effects, including akathisia. Likewise, the combination with

high-potency neuroleptics may reduce the excessive sedation associated with use of

benzodiazepines alone. However, some data support the idea that benzodiazepines alone may be as

effective as antipsychotics within the first 24 hours, even with floridly psychotic patients (Saklad et

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For less severe acute agitation, especially in a nonpsychotic patient, the use of benzodiazepines

alone appears to be adequate. Lorazepam 1–2 mg po every hour to a maximum of 10 mg or

diazepam 5–10 mg every hour to a maximum of 60 mg is usually enough to calm the more

moderately agitated patient.

A number of long-term strategies for the management of aggression in patients have been used.

Mood-stabilizing agents such as lithium, carbamazepine, and valproate have proved useful in

controlling aggressive, violent impulses in some patients. The selective serotonin reuptake

inhibitors (SSRIs) have been used with some success in studies of treating patients with aggressive

personality disorders. Likewise, buspirone, propranolol, trazodone, and clozapine, with long-term

use, may all have a role in reducing aggression in some patients.

DEPRESSION AND SUICIDALITY

Depressed, suicidal patients, along with agitated patients, represent one of the most common and

serious challenges confronted by the ER clinician. In many ERs, complaints of depression and

suicidal ideation, with or without attempts, represent the most frequent reason for psychiatric

hospital admission. Predicting imminent suicide is sometimes not an easy matter, even for skilled

psychiatrists. Many factors have been known to increase the risk of suicide, including advanced

age, a diagnosis of major depression, male gender, concurrent alcohol use, a viable suicide plan,

and a history of serious suicide attempts. The significant majority of the successful 30,000 or so

suicides that occur in the United States annually involve white males older than 45. In addition,

depression or alcohol is implicated in approximately 75% of all suicides (Bongar 1992). Fawcett et

1. (1990) attempted to further elucidate factors that may increase the immediate risk of suicide;

among these were global insomnia and severe anxiety (Table 10–2).

Table 10–2. Short-term (6- to 12-month) risk factors for suicide in depressed patients

Obsessive-compulsive features

Severe hopelessness

Panic, severe anxiety, and agitation

Global insomnia

Severe cognitive difficulties and psychotic thinking

Lack of friends in adolescence

Acute overuse of alcohol

Recurrent depression

Source. Adapted from Fawcett et al. 1990.

Suicidally depressed patients brought to an ER after suicide threats or nonharmful attempts present

a real challenge to clinical judgment. The conservative course is to admit such patients to a secure

inpatient unit. Occasionally, this may seem unwise or impractical. If the clinician can make a

relationship with and personally follow the patient, and if friends or relatives can reliably supervise

the patient until the next appointment, the patient may be referred for outpatient follow-up. In

general, any patient with suicidal ideation or attempt and depression who is psychotic, who cannot

attend to daily needs, who is acutely intoxicated, or about whose well-being the clinician has any

significant doubt should be admitted and observed.

Very few somatic interventions work rapidly enough to be useful in the emergency setting. For

example, it is generally unwise to start an antidepressant in the ER: the older antidepressants may

be lethal in overdose, the physician following the patient after the ER visit may not agree with the

ER’s choice of agents, and, in any case, it may take several weeks or longer for the antidepressant

to work. Thus, not much is lost in waiting to initiate antidepressant treatment until the patient is on

the ward or makes the first outpatient visit.

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probably underused in the emergency and acute setting for the treatment of suicidal patients.

Benzodiazepines may have an immediate effect on risk factors such as severe insomnia and

anxiety. Patients’ hopelessness is also attributed, in part, to the belief that they will never feel any

better. When they feel better quickly with a benzodiazepine, their belief system may be altered

enough to mitigate the risk of imminent suicide. We have found that lorazepam 0.5–1.0 mg qid,

with the last dose given at bedtime, can make a dramatic difference even in less agitated suicidal

patients.

A number of other somatic interventions are worth considering in the acute management of

imminently suicidal patients. Among these is electroconvulsive therapy (ECT). ECT may work very

rapidly in the profoundly depressed suicidal patient and may therefore be lifesaving. The average

number of ECT treatments for depression in the United States is eight to nine; therefore it is not

unusual to see significant benefit in the first 2 weeks of treatment. In addition, there is some

evidence that the rapid titration of some antidepressants may be associated with an earlier onset of

action. For example, premarketing studies (among them Montgomery 1993) suggested that

venlafaxine may have a more rapid onset of action when the dose is titrated up to 300 mg or more

in the first 7 days of treatment (Montgomery 1993). Unfortunately, we have found that many

patients are unable to tolerate this rapid dose titration. Other strategies that may be associated

with a more rapid onset of response for depressed suicidal patients include TCA augmentation of

SSRIs and lithium augmentation of various antidepressants.

Many depressed patients have used their antidepressants in suicide attempts. TCAs are the most

commonly used antidepressants in successful overdoses (Table 10–3). The usual cause of death in

these cases is malignant arrhythmias. Management of TCA overdoses includes charcoal lavage (50

g slurry followed by repeat doses of 25 g via nasogastric tube), admitting the patient to a unit for

cardiac monitoring, fluids to combat the adrenergic blockade, physostigmine 1 mg im for severe

anticholinergic symptoms, and correction of acidosis with sodium bicarbonate if necessary.

Table 10–3. Antidepressant overdoses and their management

Drug Toxic dose Toxicity manifestations Management

TCAs >1,500 mg

(imipramine and

most TCAs)

Anticholinergic symptoms,

arrhythmia, hypotension,

delirium, seizures

Gastric lavage, fluid support, cardiac

monitoring

MAOIs

2 mg/kg CNS excitation, hypo- or

hypertension, delirium, fever,

arrhythmia, seizures,

rhabdomyolysis

Gastric lavage, fluids, cardiac monitoring,

antihypertensives,body

cooling,benzodiazepines for CNS

symptoms, maintenance of MAOI diet

Bupropion >2 g CNS excitation, seizures Gastric lavage, benzodiazepines,

anticonvulsants

SSRIs Unknown CNS excitation, somnolence,

GI irritation

Gastric lavage, supportive care

SNRIs

(venlafaxine,

duloxetine)

Unknown Cardiotoxicity, hypertension,

seizures, serotonin effects

Gastric lavage, supportive care

Note. CNS = central nervous system; GI = gastrointestinal; MAOI = monoamine oxidase inhibitor; SNRI =

serotonin-norepinephrine reuptake inhibitor; SSRI = selective serotonin reuptake inhibitor; TCA = tricyclic

antidepressant.

MAOI overdoses of as little as 2 mg/kg may be lethal. The cause of death in MAOI overdoses

ranges from arrhythmia and cardiovascular collapse to rhabdomyolysis and renal failure. Acute

management of overdose includes gastric lavage, maintenance of MAOI diet, cardiac monitoring for

at least 24 hours, use of benzodiazepines to treat central nervous system activation, and use of

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MAOIs are also associated with another medical emergency: the development of a serotonin

syndrome. The combination of MAOIs with serotonergic drugs such as SSRIs and clomipramine (see

Chapter 3: “Antidepressants”) is among the more common causes of the serotonin syndrome.

Symptoms of the serotonin syndrome are tremor, diaphoresis, rigidity, myoclonus, and autonomic

dysregulation, potentially progressing to hyperthermia, rhabdomyolysis, coma, and death. The

treatment of serotonin syndrome involves discontinuing the offending drugs, monitoring vital signs,

and supporting vital functions. Cooling blankets are often helpful. Cyproheptadine, a general

serotonin (5-hydroxytryptamine; 5-HT) antagonist, has been used occasionally in oral doses up to

16 mg/day to counteract the serotonin syndrome. Dantrolene in doses up to 1 mg/kg iv in divided

doses has been used in severe cases to treat rigidity and prevent rhabdomyolysis. The key to

treatment of the serotonin syndrome, however, is discontinuing the offending agents and providing

supportive care.

Fortunately, many of the newer antidepressants present much less of a problem in overdose than

do the TCAs and MAOIs. Overdoses of SSRIs and 5-HT antagonists are often asymptomatic or may

present with gastrointestinal distress, agitation, and somnolence. The treatment of choice is gastric

lavage and supportive care. The British drug authorities warned that venlafaxine overdoses are

more likely to be lethal than are SSRI overdoses. Their data suggest that risk of lethality from

overdose with venlafaxine is comparable to that with TCAs. A review by the U.S. Food and Drug

Administration resulted in a change in the package insert for venlafaxine in 2006 that indicates that

venlafaxine may carry a higher risk for a fatal outcome in overdose than SSRIs but less risk than

the TCAs. The risk of fatality in overdose is not just cardiac but also associated with seizures,

rhabdomyolysis, and other causes. Patients taking venlafaxine tend to be more ill than those taking

SSRIs, and this may be associated with a greater risk of overdoses in general (Rubino et al. 2006).

One possible mechanism for the increased risk is an effect on sodium channels. Bupropion

overdoses also tend to be less dangerous than overdoses of TCAs. There has, however, been at

least one death related to neurotoxicity and seizures (see Chapter 3: “Antidepressants”).

ACUTE PSYCHOTIC REACTIONS

Psychotic symptoms can be manifestations of drug usage, mania, depression, schizophrenia,

dementia, delirium, or a variety of other disorders. An organic basis for the psychosis should be

ruled out, whenever possible, by history, physical examination, and urine and/or blood tests for

drugs of abuse.

Mixed Psychotic Reactions

With any psychotic reaction presumptively due to toxicity from illicit or licit drugs, a variety of

complicated clinical pictures can occur. Illicit drug users often take several kinds of drugs and

alcohol simultaneously. Patients with schizophrenia abuse drugs and/or become intoxicated on

alcohol, and acute drug-induced psychosis can sometimes persist and blend into a picture

indistinguishable from schizophrenia that can continue for days or weeks. The

pharmacotherapeutic problem is to choose between acute doses of an antipsychotic, a

benzodiazepine, and watchful waiting, while checking for illicit drugs in urine or blood, evaluating

possible medical causes, and obtaining a recent history from friends or relatives. Benzodiazepines

should not be used with patients who appear to be already intoxicated from alcohol or sedative

drugs.

Schizophrenic, Schizophreniform, and Manic Psychoses

When the likelihood of a drug-induced psychosis is low and the patient is manifestly acutely

psychotic—paranoid, disorganized, hallucinated, agitated, belligerent, and so forth—the rapid

tranquilization strategies described earlier are quite useful. Often oral haloperidol is taken without

objection by the patient; in that case, liquid medication is preferred, since ingestion can be

ensured.

Parenteral antipsychotics (e.g., chlorpromazine 50 mg, aripiprazole 9.75 mg, olanzapine 10–30 mg,

ziprasidone 10–20 mg, haloperidol 5–10 mg) are all effective. An antiparkinsonian drug shouldPrint: Chapter 10. Emergency Room Treatment http://www.psychiatryonline.com/popup.aspx?aID=238762&print=yes…

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usually be given at the same time as the typical antipsychotics to help avert dystonia.

Acute mania is managed with a combination of antipsychotics, benzodiazepines, and mood

stabilizers. Although loading doses of lithium have not proved useful, loading doses of valproate

may speed the onset of response. Valproate at an oral loading dosage of 20 mg/kg/day has been

associated with moderate antimanic effects occurring in as little as a few days. Standard doses of

mood stabilizers may take a week or longer to achieve adequate control of mania. Benzodiazepines

may be as useful as antipsychotics in the acute management of nonpsychotic manic patients.

However, both psychotic and nonpsychotic patients benefit equally well from an atypical agent, and

these drugs are more rapidly acting than mood stabilizers in the management of acute mania. Thus,

we will typically prescribe an atypical antipsychotic agent for a manic patient and add a

benzodiazepine or mood stabilizer as necessary.

When a psychotic patient can give some history and has a preference among available

antipsychotic drugs, or when relatives or past medical records provide relevant information, the

drug reported as best for the particular patient should be used.

Patients may present to the ER with antipsychotic complications in many forms (Table 10–4). One

still fairly common form may be the development of acute EPS. The most worrisome of the acute

EPS is dystonia. As discussed in Chapter 4 (“Antipsychotic Drugs”), young males are most

vulnerable to acute dystonic reactions, which may include oculogyric crisis, opisthotonos,

torticollis, trismus, or laryngospasm. Although all dystonic reactions are very frightening to

patients, laryngospasm compromises the airway and is potentially fatal. Severe dystonic reactions

may occur at any time of treatment, but they usually occur in the first few days of neuroleptic use.

Furthermore, high-potency typical antipsychotics may have a greater association with dystonia. The

most reliable and rapid treatment for dystonia is intravenous diphenhydramine 50 mg or

benztropine 2 mg every 30 minutes until the dystonia resolves. Laryngospasm may require

intubation and the use of intravenous lorazepam to treat the spasm. If intravenous access cannot

be secured, intramuscular injections of the drugs will be necessary. Although atypical agents are

less commonly associated with dystonic reactions, such reactions still sometimes occur.

Table 10–4. Emergency complications of antipsychotic use

Complication Risk factors Clinical findings Management

Dystonia Age < 40, male,

high-potency agents

Torticollis, opisthotonos, oculogyric

crisis, trismus, laryngospasm

Diphenhydramine (iv) or

benztropine (iv); lorazepam

and maintain airway for

laryngospasm

Overdose Age < 40, male,

educated;

schizophrenic,

psychotic depression

Hypothermia/hyperthermia, EPS,

hypotension, anticholinergic toxicity,

seizures, arrhythmia

Gastric lavage, hydration,

antiparkinsonian agents for

EPS, cardiac monitoring

Neuroleptic

malignant

syndrome

Dehydration; lithium

use; high doses

Delirium, hyperthermia, severe EPS,

autonomic instability, elevated CK

and LFTs

Stop antipsychotics;

dantrolene (iv),

bromocriptine, lorazepam

(iv)

Note. CK = creatine kinase; EPS = extrapyramidal symptoms; iv = intravenous; LFT = liver function tests.

An overdose of antipsychotics is rarely fatal. However, overdoses may result in hypothermia,

hyperthermia, severe EPS, and occasional arrhythmias. Low-potency agents may additionally

produce anticholinergic toxicity and hypotension. Hypotension is a complication of risperidone

overdose as well. All antipsychotics reduce the seizure threshold, but clozapine may be particularly

problematic in overdose. Psychotically depressed patients and young, educated male schizophrenic

patients may be at greatest risk for antipsychotic overdoses. Antipsychotic overdoses usually

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EPS, and cardiac monitoring.

NMS is a relatively rare complication of antipsychotic use that was discussed in Chapter 4. It

represents a medical emergency and is characterized by severe EPS, delirium, hyperthermia, and

autonomic abnormalities. Both typical and atypical antipsychotics, including clozapine, are

sometimes associated with NMS. The major risk factors for EPS appear to be dehydration,

concurrent use of lithium, and rapid titration to higher doses of all standard neuroleptics.

Treatment involves immediate cessation of antipsychotics, support of vital functions, and

prescription of dantrolene sodium as a muscle relaxant in doses of 0.8–1 mg/kg iv every 6 hours

for up to 2 weeks. Longer use may be associated with extreme respiratory suppression and muscle

atrophy. Bromocriptine at a dosage of up to 5 mg tid may help relieve some of the EPS, and

lorazepam 1 mg iv tid may also provide relief. In refractory cases, ECT is also reported to be of

utility.

Delirium

DSM-IV-TR (American Psychiatric Association 2000) criteria for delirium include a disturbance of

consciousness, a change in cognition, a fluctuating course, and an organic basis for the disorder.

Common causes of delirium include withdrawal syndromes, medication overdoses,

endocrinopathies, metabolic abnormalities, and infections. Very old persons appear to be at

greatest risk for the development of delirium, but it may occur at any age. The presence of delirium

is a medical emergency and is associated with significant morbidity and mortality.

Clinical management of delirium centers on assessment of the underlying cause and supportive

care. Physical restraints are often necessary and tend to be preferable to the administration of

psychoactive agents, which may further cloud the clinical picture. When medications are required

for control of an agitated, delirious patient, small doses of high-potency antipsychotics may be the

treatment of choice. Drugs such as haloperidol do not cause significant anticholinergic or

-adrenergic symptoms and tend not to present problems of cardiac or respiratory depression. A

typical dosage of haloperidol in the management of elderly delirious patients is 0.5 mg bid. Another

pharmacological option is the use of small doses of 3-hydroxy-benzodiazepines, such as lorazepam

and oxazepam, that have no active metabolites, have short half-lives, and are well metabolized

even in elderly patients. Lorazepam can be administered in doses of 0.5–1 mg iv every 30 minutes,

if administered slowly to avoid very high peak serum levels and subsequent respiratory depression.

Oxazepam is not available in a parenteral form and has the second disadvantage of slow absorption

and thus slower onset of action. If the patient is able to take medication orally, oxazepam 15 mg tid

as needed for agitation is worth considering but is generally less desirable than lorazepam. Another

strategy with which clinicians have had some success in the treatment of postoperative delirium

include gabapentin (Leung et al. 2006). Gabapentin has also been associated with reducing

perioperative pain and reducing the need for analgesics.

SEVERE ANXIETY

Patients can present with panic, severe fear and anxiety, or multiple somatic symptoms. The

symptoms of severe anxiety may be associated with a variety of medical conditions, including

hypothyroidism, hypoglycemia, coronary artery disease, carcinoid syndrome, and

pheochromocytoma. In addition, severe anxiety may be a feature of other psychiatric disorders,

including schizophrenia, acute drug intoxication, alcohol withdrawal, and depression.

The anxiety disorders with which patients are most likely to present in the ER are panic disorder

and posttraumatic stress disorder (PTSD). If medical illness can be rapidly ruled out or the patient

has a known history of panic attacks, oral diazepam offers significant advantages because of its

rapid onset of action after administration. Either 5- or 10-mg doses prn can be tried, depending on

the severity of the anxiety and the patient’s past responses to sedatives. If intramuscular

administration is required, however, diazepam is not an ideal choice because of its erratic

absorption. Lorazepam and midazolam are the only benzodiazepines reliably absorbed from the

intramuscular route. Lorazepam 1 mg im repeated hourly is effective in the acute management ofPrint: Chapter 10. Emergency Room Treatment http://www.psychiatryonline.com/popup.aspx?aID=238762&print=yes…

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severe anxiety. Antidepressant drugs are indicated in the longer-term treatment of panic disorders,

but they are slow in onset and of no immediate value in patients experiencing acute, severe

anxiety. Thus, it may be appropriate to use a benzodiazepine with an antidepressant in the initial

weeks of antipanic therapy. A month later, the benzodiazepine may be tapered off after the

antidepressant has begun to work. Clonazepam is also an effective antipanic agent and can be

initiated at a dosage of 0.5 mg bid. Although anticonvulsants such as gabapentin and tiagabine are

occasionally useful, they do not appear to be as rapidly acting as the benzodiazepines.

PTSD patients may present to the ER with significant symptoms of autonomic arousal from

flashback experiences, intrusive thoughts, and insomnia. It is important to evaluate patients for

comorbid disorders such as depression and substance abuse. Violent or agitated PTSD patients

should be managed by the rapid tranquilization methods described earlier. -Blockers may also be

helpful in the initial management of autonomic hyperarousal. However, long-term treatments,

including the use of antidepressants and mood-stabilizing agents, are best initiated after the acute

distress is reduced and long-term follow-up is secured.

Some experts prefer low-dose antipsychotic drugs in patients with borderline or other personality

disorders who present in an acute crisis. If the patient has a past history of sedative abuse,

olanzapine 5–10 mg or chlorpromazine could be used. Chlorpromazine’s sedation is likely to persist

for many hours—at times, longer than is desired. If the patient is currently dependent on sedative

drugs, consideration must be given to the problem of withdrawal reactions if the drugs are stopped

abruptly. Buspirone is available for use in anxiety, but single doses are not helpful in reducing

acute symptoms.

STUPOR AND CATATONIA

Catatonia is a syndrome that may be induced by a variety of medical and psychiatric disorders. It is

characterized by cataplexy and waxy flexibility, mutism, resistance to instructions or attempts to

be moved (negativism), and intermittent agitation. The causes of catatonia range from metabolic

disorders such as hepatic encephalopathy and ketoacidosis to postictal states and basal ganglia

lesions. Affective disorders represent the most common psychiatric cause of catatonia, although

the syndrome often occurs in schizophrenia.

Nonpsychiatric etiologies account for a large percentage of catatonia cases. Therefore, a thorough

history, a physical examination, and laboratory assessment are required. If medical or neurological

causes for stupor can be ruled out, hospital admission to a psychiatric ward is generally indicated.

If no information on the patient is available, intravenous amobarbital sodium can sometimes

facilitate obtaining a history by letting the patient talk relatively freely. However, this approach

requires the clinician to be experienced in the technique, and, again, it is best done in an inpatient

setting (see Chapter 6: “Antianxiety Agents”). Intravenous amobarbital sodium is given at a rate

up to 50 mg/minute to a maximum of 700 mg. The dose is titrated to the size and age of the

patient; smaller and older patients require smaller amounts. There is a significant risk of

respiratory depression with larger doses, which necessitates having a crash cart available and

perhaps having a second IV line in case of difficulties. Parenteral lorazepam (1–2 mg) appears

safer than amobarbital, and it may also facilitate the patient’s ability to give a history.

There are lethal forms of catatonia in which patients present with hyperthermia, extreme rigidity,

mental status changes, muscle breakdown, rhabdomyolysis, and renal failure. This so-called lethal

or malignant catatonia may be quite difficult to distinguish from NMS. The distinction may be

important, because lethal catatonia sometimes responds to antipsychotics, whereas antipsychotics

are contraindicated in treating NMS. Fortunately, both NMS and lethal catatonia may respond to

ECT.

EMERGENCY ROOM REFERRALS

Psychiatric patients are occasionally referred to a general hospital ER by their psychiatrist after

telephone calls or office visits. Definite or possible overdose attempts, unexplained confusional

states, or serious drug side effects (such as MAOI-related hypertensive crises or acute dystonia)Print: Chapter 10. Emergency Room Treatment http://www.psychiatryonline.com/popup.aspx?aID=238762&print=yes…

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are reasonable examples of appropriate referrals.

It is important for psychiatrists to remember that ER physicians may know less about the

pharmacological effects of psychiatric drugs than they do, despite the natural hope that the ER

doctor will be all-knowing and highly resourceful. Therefore, to ensure that no major gaps in

knowledge exist, it is worthwhile to call the ER before the patient gets there and/or after the

patient has been initially evaluated. Many physicians have never heard that meperidine can be fatal

when added to an MAOI. Some who do not know that TCAs have quinidine-like effects on cardiac

conduction might give quinidine to treat an arrhythmia resulting from TCA overdose. Not

uncommonly in ERs, a patient with a severe headache due to a hypertensive crisis may be ignored

(i.e., made to wait) until the headache has passed on its own.

If a patient is sick enough to be admitted to a hospital and the psychiatrist knows of a history of

benzodiazepine use, the psychiatrist should encourage the hospital staff to be concerned about

withdrawal symptoms such as seizures or delirium. Also, the emergency physician may be

reassured to know that overdoses of SSRIs, serotonin2 (5-HT2) antagonists, venlafaxine, and

bupropion are likely to be relatively benign. In our experience, ER staff seem interested and

appreciative when the responsible psychiatrist calls and provides both clinical and

psychopharmacological input.

BIBLIOGRAPHY

American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, 4th

Edition, Text Revision. Washington, DC, American Psychiatric Association, 2000

Andrezina R, Josiassen RC, Marcus RN, et al: Intramuscular aripiprazole for the treatment of acute

agitation in patients with schizophrenia or schizoaffective disorder: a double-blind,

placebo-controlled comparison with intramuscular haloperidol. Psychopharmacology (Berl)

188:281–292, 2006a

Andrezina R, Marcus RN, Oren DA, et al: Intramuscular aripiprazole or haloperidol and transition to

oral therapy in patients with agitation associated with schizophrenia: subanalysis of a double-blind

study. Curr Med Res Opin 22:2209–2219, 2006b

Bazire S: MAOIs and narcotic analgesics (letter). Br J Psychiatry 151:701–710, 1987 [PubMed]

Bongar B: Suicide Guidelines for Assessment, Management and Treatment. New York, Oxford

University Press, 1992

Breier A, Wright P, Birkett M, et al: Intramuscular olanzapine: dose-related improvement in acutely

agitated patients with schizophrenia. Presentation at the 154th annual meeting of the American

Psychiatric Association, New Orleans, May 5–10, 2001

Browne B, Lintner S: Monoamine oxidase inhibitors and narcotic analgesics: a critical review of the

implications for treatment. Br J Psychiatry 151: 210–212, 1987 [PubMed]

Cole J: Drugs and seclusion and restraint. McLean Hospital Journal 10:37–53, 1985

Crome P: Antidepressant overdosage. Drugs 23:431–461, 1982 [PubMed]

Dubin WR, Field JA: Rapid tranquilization of the violent patient. Am J Emerg Med 7:313–319, 1989

[PubMed]

Dubin W, Stolberg R: Emergency Psychiatry for the House Officer. New York, SP Medical & Scientific

Books, 1981

Dubin WR, Waxman MH, Weiss KJ, et al: Rapid tranquilization: the efficacy of oral concentrate. J

Clin Psychiatry 46:475–478, 1985 [PubMed]

Fawcett J, Scheftner WA, Clark DC: Time related predictors of suicide. Am J Psychiatry

147:1189–1194, 1990 [PubMed]

Goldberg RJ, Dubin WR, Fogel BS: Behavioral emergencies: assessment and psychopharmacologicPrint: Chapter 10. Emergency Room Treatment http://www.psychiatryonline.com/popup.aspx?aID=238762&print=yes…

11 of 11

31/01/2009 06:55

management. Clin Neuropharmacol 12:233–248, 1989 [PubMed]

Hillard JR (ed): Manual of Clinical Emergency Psychiatry. Washington, DC, American Psychiatric

Press, 1990

Hughes DH: Trends and treatment models in emergency psychiatry. Hosp Community Psychiatry

44:927–928, 1993 [PubMed]

Hyman SE, Tesar GE: Manual of Psychiatric Emergencies, 3rd Edition. Boston, MA, Little, Brown,

1994

Lavoie FIV, Carter GL, Danzl DF, et al: Emergency department violence in United States teaching

hospitals. Ann Emerg Med 17:1227–1232, 1988 [PubMed]

Leung JM, Sands LP, Rico M, et al: Pilot clinical trial of gabapentin to decrease postoperative

delirium in older patients. Neurology 67:1251–1253, 2006 [PubMed]

Meehan KM, Zhang F, David SR, et al: A double-blind, randomized comparison of the efficacy and

safety of intramuscular injections of olanzapine, lorazepam, or placebo in treating acutely agitated

patients diagnosed with bipolar mania. J Clin Psychopharmacol 21:389–397, 2001 [PubMed]

Meehan KM, Wang H, David SR, et al: Comparison of rapidly acting intramuscular olanzapine,

lorazepam, and placebo: a double-blind, randomized study in acutely agitated patients with

dementia. Neuropsychopharmacology 26:494–504, 2002 [PubMed]

Moller HJ, Kissling W, Lang C, et al: Efficacy and side effects of haloperidol in psychotic patients:

oral vs. intravenous administration. Am J Psychiatry 139:1571–1575, 1982 [PubMed]

Montgomery SA: Venlafaxine: a new dimension in antidepressant pharmacotherapy. J Clin

Psychiatry 54:119–124, 1993

Munizza C, Furlan PM, d’Elia A, et al: Emergency psychiatry: a review of the literature. Acta

Psychiatr Scand Suppl 374:1–51, 1993 [PubMed]

Puryear DA: Proposed standards in emergency psychiatry. Hosp Community Psychiatry 43:14–15,

1992 [PubMed]

Rubino A, Roskell N, Tennis P, et al: Risk of suicide during treatment with venlafaxine, citalopram,

fluoxetine, and dothiepin: retrospective cohort study. BMJ December 12, 2006 [Epub ahead of

print]

Saklad SR, Ereshefsky L, Jann MW, et al: Usefulness of injectable and oral lorazepam in psychotic

and developmentally disabled patients. Paper presented at the 138th annual meeting of the

American Psychiatric Association, Dallas, TX, May 20–23, 1985

Szuster RR, Schanbacher BL, McCann SC, et al: Underdiagnosis of psychoactive-substance-induced

organic mental disorders in emergency psychiatry. Am J Drug Alcohol Abuse 16:319–327, 1990

[PubMed]

Weissberg MP: Emergency psychiatry: a critical educational omission (editorial). Ann Intern Med

114:246–247, 1991 [PubMed]

Wright P, Lindberg SR, Birkett M, et al: Intramuscular olanzapine and intramuscular haloperidol in

acute schizophrenia: antipsychotic efficacy and extrapyramidal safety during the first 24 hours of

treatment. Can J Psychiatry 48:716–721, 2003 [PubMed]

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